This preclinical study suggests that Na(+)-Ca2+ exchange is the primary mechanism for calcium entry and subsequent myocardial damage during the calcium paradox.
Hypothesis-generating for Na(+)-Ca2+ exchange blockade in calcium paradox; clinical translation requires prospective validation.
The damage done to Langendorff perfused guinea-pig hearts by initiation of a calcium paradox, as assessed by the loss of myoglobin, is significantly reduced if inhibitors of Na(+)-Ca2+ exchange (Mn2+, Ni2+, bepridil and dodecylamine) are present when Ca2+ is repleted. This protection is not, to any major extent, due to secondary effects of these agents on the L-type Ca2+ channels, because more specific inhibitors of the Ca2+ channels are much less effective. These results suggest that the principal route for Ca2+ entry during the calcium paradox is Na(+)-Ca2+ exchange.
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Chatamra et al. (1996) studied this question.
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